INVESTIGADORES
FOSSATI Carlos Alberto
congresos y reuniones científicas
Título:
The potential role of inflammatory immune response in Brucella dissemination from the lung
Autor/es:
HIELPOS S; FERRERO MC,; FOSSATI, CA; BALDI PC,
Reunión:
Congreso; First French-Argentine Immunology Congress. LVIII Reunión Anual de la Sociedad Argentina de Inmunología; 2010
Resumen:
Brucella
is a human pathogen that can be acquired by inhalation. We investigated
potential mechanisms by which Brucella may cross the pulmonary epithelial
barrier (transcellular or paracellular passage, and transmigration of infected
phagocytes or "Trojan horse mechanism"). We used the normal human
bronchial epithelial cell line 16HBE14o- which forms a polarized monolayer when
grown on filters. B. abortus 2308 invaded and also replicated in 16HBE14o-
polarized monolayers (99.5 ± 22, 499.5 ± 47.5, 3093.5 ± 12812.5 CFU/well at 2,
24 and 48 h pi, respectively). However, it failed to make either transcellular
passage through the monolayer (no bacteria detected in the lower compartments
until 48 h p.i) or paracellular passage (no bacteria detected at 4 h after placing
B. abortus in the upper compartment). In these experiments, FITC-albumin, added
together with the inoculum, did not cross the epithelial barrier indicating
preservation of both membrane integrity and intercellular junctions. Since no
direct translocation of the epithelial barrier was observed, we decided to
evaluate if Brucella induces an epithelial inflammatory response that could
induce transepithelial migration of infected phagocytes. Infection with both
the smooth strain B. abortus 2308 or the rough strain B. abortus RB51 induced
the production of IL-8, GM-CSF but not MCP-1, IL-1 and TNF-α. The specific
levels of IL-8 in
culture supernatants of infected cells with smooth or rough strains were 3348
±127.8 pg/ml and 3645.5 ± 74.4 pg/ml, and for GM-CSF were 57.4 ± 15.0 pg/ml and
163.89 ± 20.52 pg/ml respectively at 48 h p.i. Neither Brucella LPS nor heat
killed bacteria induced these responses.These results indicate that B. abortus
does not translocate the lung epithelial barrier by direct passage but is
likely to do so by mechanisms related to the inflammatory response triggered by
the infection.